Researchers who work on autophagy might well feel justified in issuing the claim that the processes of autophagy are involved in near every aspect of aging. Autophagy is cellular housekeeping, the recycling of damaged or unwanted structures and molecules inside the cell. In chaperone-mediated autophagy, very selective chaperone proteins pick up other molecules and carry them to lysosomes. In macroautophagy, materials to be broken down are engulfed in an autophagosome, which then travels to the lysosome and fuses with it. In microautophagy, the lysosome engulfs materials directly. In all cases, the lysosome is the end of the journey, where a mix of enzymes will slice up the waste material into parts suitable for reuse. The result of smoothly running autophagy is a cell that is less cluttered with damaged parts and waste, and thus a cell that causes fewer issues to the tissue it is a part of.
This business of keeping molecular wear and tear inside cells to a minimal level appears a noteworthy determinant of aging. Many of the methods shown to slow aging in laboratory species such as flies, nematodes, and mice involve increased autophagy. Cells react to stress by
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